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Clerk GCP
Clerk GCP
Clerk GCP
Specific objectives:
1) To present an approach to patient who came in due to shortness of breath.
2) To present the epidemiology, pathophysiology and pathogenesis of Human Immunodeficiency
Virus/Acquired Immunodeficiency Syndrome (HIV/AIDS).
3) To present the pathogenesis, clinical manifestations, diagnosis and management of Pneumocystis
Pneumonia as a complication of HIV/AIDS.
GENERAL DATA
A case of JD, 25 year old male, Filipino, Roman Catholic, single, currently unemployed, from Purok
1, Kalubihon, Dalifuga, Iligan City. This is his first hospital admission in this institution. The source of
information was the patient himself with 95% reliability.
2
take-home medications of Cefixime 400 mg tablet 1 tab BID for 10 days, Fluconazole 50mg capsule 1 cap
OD for 7 days, Azithromycin (Natrapharm) 500 mg tablet 1 tab OD for 10 days, Cotrimoxazole 800mg tablet
1 tab BID for 10 days and Prednisone 20 mg tablet 1 tab BID after meals for 10 days with good compliance.
Patient was advised to undergo HIV counselling.
4 days PTA, patient was afebrile but still with occasional productive cough, yellowish sputum and
shortness of breath on exertion upon climbing 5 steps of stairs. Patient continued taking take-home
medications. No consult was done.
2 days PTA, patient sough consult at City Hospital TB DOTS, sputum AFB was done with pending
results. There was noted recurrence of fever in the afternoon that day. Patient self-medicated with
Paracetamol 500 mg 1 tab every 4 hours taken for fever along with the prescribed home medications.
1 day PTA, patient went for HIV counselling and testing at City Health. Patient lost consciousness
upon learning he was reactive to initial HIV screening, but regained consciousness after 1 minute. He noted
shortness of breath even during changing clothes, with undocumented fever and occasional productive
cough. Persistence and worsening of condition prompted consult and subsequent admission.
FAMILY HISTORY
The patient has a familial history of hypertension from his paternal side, and a history of thyroid
and heart disease from his maternal side.
REVIEW OF SYSTEMS
General: No unintentional weight loss, no loss of appetite, weakness, or fatigue
Skin: No rashes, itching, changes in hair and nails.
Head: No headache or dizziness
Eyes: No blurring of vision
Ears: No difficulty hearing, tinnitus, vertigo, or otalgia
Nose and sinuses: No nasal stuffiness, discharge or itching, or epistaxis
Throat: No dysphagia or odynophagia
Neck: No stiffness
Respiratory: No colds, no hemoptysis
Cardiovascular: No orthopnea, no palpitations, no chest pain or discomfort
Gastrointestinal: No abdominal pain or changes from normal bowel movement, no melena or
hematochezia
Genitourinary: No dysuria, hematuria, or penile discharges
Endocrine: No heat or cold intolerance, no tremors, no palpitations
Hematologic: No easy bruisability or active bleeding
Neurology: No seizures, loss of consciousness or changes in behaviour
3
PHYSICAL EXAMINATION
General survey
Patient is examined on the first hospital day.
Patient is awake, conscious, well-dressed, sthenic built with supplemental oxygen at 4LPM via nasal
cannula. He is oriented, cooperative, lying supine and in respiratory distress, able to speak in phrases.
Vital signs
Blood pressure: 90/60 mmHg
Pulse rate: 110 bpm
Respiratory rate: 26 cpm
Temperature: 38.2oC, Left axilla
O2 sat: 90% at O2 inhalation 4LPM
Anthropometrics
Height: 165 cm
Weight: 81 kg
BMI: 29.75 kg/m2 (Asia-Pacific Classification: Obese class 1)
Skin
Inspection:
Patient has brown skin. There are no rashes, bruises, ulcerations, cyanosis or jaundice noted. No
palmar erythema, spider angiomata noted.
Palpation:
Skin is warm to touch with smooth texture. There is good skin turgor and no tenderness noted.
Nails
Inspection:
He has pink nail beds on both upper and lower extremities. No nail clubbing and indentions.
Palpation:
Capillary refill time <2 seconds on all extremities.
HEENT
Inspection:
Normocephalic, no facial asymmetry.
Hair is short, fine, black and evenly distributed. There are no lesions seen on the scalp.
He has anicteric sclera and pink palpebral conjunctivae.
No nasal discharge.
Dry lips and moist oral mucosa. No oral lesions.
No tonsillopharyngeal enlargement.
Non-distended neck veins noted. No visible mass and pulsations.
Palpation:
There are no masses, no tenderness or lymphadenopathy noted.
4
Thorax is symmetrical. There is equal chest expansion with no chest lag and intercostal/ subcostal
retractions. No lesions, lumps and masses noted.
Palpation:
Normal tactile and vocal fremeti in both lung fields.
Percussion:
Resonant lung fields.
Auscultation:
There were fine rales, bibasal, more on the right. Bronchophony, egophony, whispered
pectoriloquy are all absent.
Cardiovascular System
Inspection:
He has adynamic precordium. Point of maximal impulse is noted at the 5th intercostal space,
midclavicular line, left.
Palpation:
There are no thrills and heaves noted. Apex beat felt at the 5th intercostal space, midclavicular line,
left.
Auscultation:
He has distinct s1 and s2, tachycardic with regular rhythm. No murmurs noted.
Abdomen
Inspection:
Abdomen is flabby with no visible veins, pulsations, or lesions.
Auscultation:
Normoactive bowel sounds at 12/clicks per minute.
Percussion:
Tympanitic except over the area of the liver. Liver span is 8cm, midclavicular line.
Palpation:
No tenderness on both light and deep palpation. There is no hepatomegaly and spleen is not
palpable. No masses noted.
Genitourinary system
Inspection:
Grossly male. Multiple papulonodular lesion of varying sizes, pinkish to brown in color, located on
the dorsal and lateral shaft and base of the penis. No ulcers or scars noted on the glans, shaft and base of
the penis as well as on scrotal surface. No penile discharges noted.
Palpation:
No tenderness, induration noted on the penile area. No tenderness or swellings on the scrotum.
No inguinal lymphadenopathy.
Extremities
Inspection:
No lesions and no edema. No deformities.
5
There are full pulses on all extremities.
Musculoskeletal System
Inspection:
He has good symmetric muscle bulk and tone. No deformities, atrophies, spasticity and joint
swelling noted.
Nervous System
Mental State: Oriented to time, place, and persons and responds appropriately.
Cranial Nerves:
CN I: Not assessed
CN II: Visual acuity and Visual fields intact.
CN III, IV, VI: No ptosis. Extraocular movements were intact.
CN V: Able to open and close mouth. Can identify light touch on both cheeks, forehead and
mandibular area. Positive Corneal reflex.
CN VII: Able to raise eyebrows; no facial asymmetry noted.
CN VIII: Able to hear whispers and spoken words on both ears.
CN IX, X: Able to swallow, no deviation in uvula, intact gag reflex.
CN XI: Able to shrug both shoulders against resistance, able to turn head left and right.
CN XII: Tongue protrudes at midline.
Motor:
Right Left
Cerebellar: Able to do rapid alternating movements; able to do finger to nose; normal gait
Sensory: Intact sensation on light touch, pain, temperature and pin prick.
Reflexes:
6
SALIENT FEATURES
APPROACH TO DSYPNEA
Dyspnea is a subjective experience of breathing discomfort that consist of qualitatively distinct
sensations that vary in intensity. Evaluation of patients with dyspnea includes history which should be
described in the patient’s own words, physical examination to further investigate, and laboratory
procedures to confirm the findings.
An algorithm for the evaluation of patient presenting with dyspnea starts with history taking,
considering the quality of sensation, timing, positional disposition and whether dyspnea is intermittent or
persistent1. In relation to this case, it is important to note that the patient is already experiencing
intermittent productive cough of 1 month duration associated with progressive dyspnea and fever which
usually occurred in the afternoon. Patient noticed his dyspnea was persistently progressive, aggravated
upon febrile episodes and upon exertion of 5 stair steps. Patient was recently admitted, managed as a case
of CAP-MR, however went home against medical advice due to unimproved condition. Patient was Reactive
upon initial HIV testing.
After taking the history, it is important to perform a thorough physical examination. Evidence of
increased work of breathing like supraclavicular retractions; use of accessory muscles of ventilation; and
the tripod position indicate stiffness of the lungs or the chest wall1. The patient was examined in distress,
able to speak in phrases. No retractions, use of accessory muscles or tripod position. During the general
examination, signs of anemia, cyanosis, and cirrhosis should be sought. This patient has pink palpebral
conjuctivae, no pallor, palmar erythema, nor spider angiomata noted.
Examination of the chest should focus on symmetry of movement; palpation of both tactile and vocal
fremitus, percussion and auscultation1. In this case, the patient has symmetrical chest, equal chest
expansion, normal tactile and vocal fremiti and bibasal rales, more on the right which makes it likely that
there is a pulmonary etiology of dyspnea.
The cardiac examination should focus on signs of elevated right heart pressures, left ventricular
dysfunction and valvular disease1. The patient doesn’t have jugular venous distention, JVP is 7cmH2O, no
s3 or s4 gallops and no murmurs heard. This may indicate that a cardiac cause of dyspnea is less likely.
When examining the abdomen, paradoxical movement of the abdomen should be noted which is a
sign of diaphragmatic weakness and rounding of the abdomen that suggest pulmonary edema 1 which are
both absent in the patient, making pulmonary edema less likely.
7
Examination of the extremities should take note of edema, cyanosis, any deformities, as well as
clubbing of digits, which is an indication of interstitial pulmonary fibrosis1. For this patient, examination of
the extremities were unremarkable.
After a thorough history taking and physical examination, possible diagnosis may be evident. For this
case we are highly considering a pulmonary cause of the dyspnea given the pertinent physical findings of
chest and lungs. However, further evaluation can be done through chest radiograph where cardiac size,
any evidence of CHF, hyperinflation, possible pneumonia, interstitial lung disease and pleural effusion can
be assessed to aid in narrowing the differentials diagnosis and most importantly to arrive at the correct
diagnosis. ECG and echocardiography, pulmonary function testing, and haematocrit and thyroid function
tests may be utilized to further narrow down or confirm the diagnosis. If still uncertain, cardiopulmonary
exercise test may be used1.
FORMULATION
Presented with a case of 25-year old male, who came in due to shortness of breath, with history of
5 male sexual partners with unprotected anal and oral sexual practices, productive cough for 1 month with
8
yellowish sputum, intermittent fever associated with reactive result in initial HIV screening and upon
physical examination, the patient was tachycardic at 110bpm, tachypneic at 26cpm, febrile at 38.2 C, with
equal chest expansion, normal tactile and vocal fremiti, bibasal fine rales, more on the right and absence
of bronchophony, egophony and whispered pectoriloquy.
DIFFERENTIAL DIAGNOSIS
1) Pneumocystis Pneumonia
2) HIV Clinical Stage III
3) Genital Warts
9
40 mg tab 1 tab BID. O2 support was ordered via nasal cannula at 2-4 LPM. The
patient was ordered with a diet as tolerated at 1500 kCal/day in 3 divided meals
and 2 snacks with strict aspiration precaution, with a distribution of 60%
carbohydrates, 20% protein and 20% fats.
Problem #1: Pneumocystis Pneumonia (PCP), Human Immunodeficiency Virus (HIV)
Hospital Day 1 Patient was seen awake, coherent, in respiratory distress. Patient had productive
cough with yellowish phlegm and complained of shortness of breath. He was noted
to be tachycardic at 100 bpm, tachypneic at 26 cpm, febrile at 38.2 C, with an O2sat
of 85% under O2 support via nasal cannula. Patient was on PNSS 2L at 20 gtts/min,
with an input of 2900 ml and an output of 2640 ml. Physical examination showed
anicteric sclerae, pink palpebral conjuctivae, and pupils equally round and reactive
to light and accommodation; equal chest expansion, bibasal rales (more on the
right); adynamic precordium, regular rhythm, with no murmurs; flabby abdomen,
normoactive bowel sounds, soft, non-tender; full peripheral pulses with no edema;
muscle strength of 5/5 in all extremities. Laboratory findings revealing leukocytosis
of 18.41 x103/ul with predominant neutrophils of 89.80%, low hematocrit count of
36.70%, and a high platelet count of 483 x103/ul; an elevated BUN of 35.43, and
creatinine of 0.72; Chest X-ray AP view revealed fine reticular and alveolar densities
seen within both lungs suggesting bilateral Pneumonia.
Hospital Day 2 Patient had shortness of breath and occasional cough productive yellowish phlegm,
no febrile episodes. Medications ordered were continued. On the 3rd hospital day,
patient shortness of breath improved but still with occasional cough. No febrile
episodes noted. Equal chest expansion was noted but with findings of rales on both
lung fields, more on the right. Blood chemistry was requested revealing
unremarkable FBS, cholesterol, and triglycerides. Complete blood count revealed
leukocytosis of 14.12 x103/ul with predominant neutrophil of 94.30% and elevated
platelet count of 553 x103/ul. Patient was advised to have Chest Xray-PAL and
Ultrasound of the whole abdomen. Medications were continued.
Hospital Day 4 Shortness of breath improved but still with coughing episodes. Upon physical
examination, patient’ rales on both lung fields decreased but noted decreased
breath sounds on bibasal lung fields. X-ray of the chest taken in PAL view revealed
minimal progression of previously noted air space opacities in both lungs suggesting
10
worsening bilateral Pneumonia. Microbiology examination of blood after 3 days
incubation revealed no growth. Medications were continued.
Hospital Day 5 to 8 Patient’s shortness of breath and cough improved. Upon physical examination,
patient rales decreased but decreased breath sounds were still noted on bibasal
lung fields. On the 8th hospital day, Salbutamol + Ipatropium bromide nebulization
every 15 minutes for 3 doses was ordered, then every 8 hours. Other medications
were continued.
Problem #2: Genital Warts
Hospital Day 1 During physical examination, the patient was noted to have multiple papulonodular
lesions of varying sizes, rounded in shape on the dorsal aspect of the penis. No
associated tenderness on the affected area, no ulcers, scars, nodules, or signs of
inflammation noted on the skin, foreskin, glans and base of the penis as well as on
scrotal surface. No discharges noted. The lesions were identified as genital warts.
No medications were ordered for this.
Hospital Day 2 to 9 Genital lesions were still noted without any change in number, distribution, location
and characteristics of the lesions and without any associated symptom. Still, no
medication was ordered for the lesion.
Hospital Day 4 Patient noticed to have onset of oral lesion located in the soft palate. There was no
associated pain at the site of the lesions, itchiness, difficulty swallowing or any bad
taste sensation. The lesions were characterized as thick small annular plaques, few
in number having asymmetric distribution localized in the soft palate, with well-
defined borders, creamy white in color, non-erythematous, about 3 mm in greatest
dimension without bleeding or exudates. The lesions were then identified as oral
thrush. Fluconazole 200 mg 1 tab once a day was then started. Other medications
were continued.
Hospital Day 5 On the 5th hospital day, still with no pain, itchiness, difficulty swallowing or any
change in taste sensation was noted. The lesions had increased in number now
affecting the buccal and inner lip mucosa as well having a 6 mm greatest dimension,
without bleeding or exudates. Fluconazole was continued.
Hospital Day 7 On the 7th hospital day, oral thrush was still present with no associated pain,
itchiness, difficulty swallowing or any change in taste sensation. The lesions were
noted to have decreased in number, now only affecting the soft palate and buccal
mucosal area without extension to the pharyngeal area. Ongoing medications were
continued. No new medication was added.
11
Hospital Day 8 On the 8th hospital day, oral thrush was still noted without any associated
symptoms. The lesions became localized in the soft palate, few in number without
redness, bleeding or exudates. Fluconazole was still continued.
Hospital Day 9 On the 9th hospital day, complete resolution of the lesion was noted. No
pain, itchiness, or redness was noted. Fluconazole was still continued.
On the 8th hospital day, oral thrush was still noted without any associated symptoms. The lesions
became localized in the soft palate, few in number without redness, bleeding or exudates. Fluconazole
was still continued.
On the 9th hospital day, complete resolution of the lesion was noted. No pain, itchiness, or redness
was noted. Fluconazole was still continued.
CASE DISCUSSION
Epidemiology
HIV infection is a global pandemic, with cases reported from virtually every country. At the end
of 2013, an estimated 35.0 million individuals were living with HIV infection1 . An estimated 95% of
people living with HIV/AIDS reside in low and middle-income countries; ~50% are female, and 3.2 million
are children <15 years. In 2013, an estimated 2.1 million new cases of HIV infection occurred worldwide,
including 240,000 among children <15 years; about 40% of new infections were among persons under
age 25.
The HIV epidemic has occurred in “waves” in different regions of the world, each wave having
somewhat different characteristics depending on the demographics of the country and region in
question and the timing of the introduction of HIV into the population.
In Asia and the Pacific, an estimated 4.8 million people were living with HIV at the end of 2013. In
this region of the world, HIV prevalence is highest in Southeast Asian countries, with wide variation in
trends between different countries.
12
In the Philippines2, there were 924 new HIV antibody seropositive individuals reported to the
HIV/AIDS & ART Registry of the Philippines (HARP). Nineteen percent (179) had clinical manifestations
of advanced HIV infection (WHO clinical stage 3 or 4) at the time of diagnosis. Ninety-six percent (885)
of the newly diagnosed were male. The median age was 28 years old and half (50%) were 25-34 years
old at the time of testing. About one third (30%) were from National Capital Region and less than 1%
were from ARMM. Sexual contact remains the predominant mode of transmission. Among this, eight-
six percent were males who have sex with males (MSM). Other mode of transmission was needle sharing
among injected drug users (1%).
13
Once infection is established, the virus replicates in lymphoid cells in the mucosa, the submucosa,
and to some extent the lymphoreticular tissues that drain the gut tissues. In acute HIV syndrome, which
occurs in ~50% of individuals, acute mononucleosis-like symptoms are well correlated with the presence
of Viremia. Once infection has been established the virus succeeds in escaping complete immune-
mediated clearance, paradoxically seems to thrive on immune activation, and is never eliminated
completely from the body. Most patients are relatively asymptomatic while this progressive decline of
CD4 T cells is taking place and are often described as being in a state of clinical latency. A chronic
infection develops and persists with varying degrees of continual virus replication in the untreated
patient for a median of ~10 years before the patient becomes clinically ill. It is this establishment of a
chronic, persistent infection that is the hallmark of HIV disease. Once patients reach CD4+ T cell levels
below a critical level of (<200/μL), they are at high risk of developing a variety of opportunistic diseases,
For this reason, the CDC case definition of AIDS includes all HIV-infected individuals over 5 years of age
with CD4+ T cell counts below this level. The depletion of CD4+ T cells continues to be progressive and
unrelenting in this phase.
Epidemiology
Pneumocystis pneumonia (PCP) remains the most prevalent opportunistic infection in patients
infected with the human immunodeficiency virus (HIV). 4 PCP is caused by Pneumocystis jirovecii, an
organism classified as a fungus but also shares biologic characteristics with protozoa. Pneumocystis
spreads by the airborne route, occurring by new acquisition or reactivation of infection. 5
The incidence of PCP has declined substantially with widespread use of PCP prophylaxis and
antiretroviral therapy (ART), compared before when PCP occurred in 70% to 80% of patients with AIDS,
and these patients were associated with a 20% to 40% mortality rate in individuals with profound
immunosuppression. 6
Approximately 90% of PCP cases occurred in patients with CD4 T-lymphocyte (CD4 cell) counts
<200 cells/mm3. Higher risk of PCP includes CD4 cell percentage <14%, previous episodes of PCP, oral
thrush, recurrent bacterial pneumonia, unintentional weight loss, and higher plasma HIV RNA levels.
14
Most cases occur in patients who are unaware of their HIV infection or are not receiving ongoing care
for HIV, and in those with advanced immunosuppression (CD4 counts <100 cells/mm3). 7
Clinical Manifestations
Pneumocystis pneumonia is often the AIDS-defining illness in patients infected with HIV,
occurring most frequently when the T-helper cell count (CD4+) is less than 200 cells per cubic
millimeter. 4 In HIV-infected patients, the most common manifestations of PCP are sub-acute onset of
progressive 4dyspnea, fever, non-productive cough, and chest discomfort that worsens within days to
weeks. The fulminant pneumonia observed in patients who are not infected with HIV is less common.
In mild cases, pulmonary examination usually is normal at rest. With exertion, tachypnea, tachycardia,
and diffuse dry rales may be observed. 8
Oral thrush is a common co-infection. Fever is apparent in most cases and may be the
predominant symptom in some patients.9 Hypoxemia, the most characteristic laboratory abnormality,
can range from mild (room air arterial oxygen [pO2] ≥60 mm Hg) to moderate (40-59 mm Hg) to severe
(<40 mm Hg). Elevation of lactate dehydrogenase levels to >500 mg/dL is common but non-specific. 7
Chest radiograph typically demonstrates bilateral perihilar interstitial infiltrates that become
increasingly homogeneous and diffuse as the disease progresses. Less common findings include solitary
or multiple nodules, upper-lobe infiltrates in patients receiving aerosolized pentamidine,
pneumatoceles, and pneumothorax. Pleural effusions and thoracic lymphadenopathy are rare. 8
Spontaneous pneumothorax in a patient with HIV infection should raise the suspicion of approximately
13% to 18% of patients with documented PCP have another concurrent cause of pulmonary
dysfunction, such as tuberculosis (TB), Kaposi sarcoma (KS), or bacterial pneumonia. 7
Diagnosis
The principal definitive diagnosis for Pneumocystis infection remains direct visualization of the
pathogen by various staining techniques such as the Grocott-Gomori methenamine silver (GMS),
Wright-Giemsa, calcofluor white, and the Papanicolaou stains.10 Spontaneously expectorated sputum
has low sensitivity and should not be submitted to the laboratory to diagnose PCP.
Direct and indirect immunofluorescent stains that utilize antibodies directed against the
organism are also commonly used.12 GMS selectively stains the wall of Pneumocystis cysts and can be
used on smears or tissue (Fig. 1). Wright-Giemsa stains all stages of the parasite and works best with
cytologic smears. Calcofluor white is a chemifluorescent agent that nonspecifically binds to the b-linked
polymers of the cell wall and can be used with tissue or smears. The Papanicolaou stain highlights the
eosinophilic material surrounding the organism known as a ‘‘foamy body’’ but does not stain individual
organisms clearly.10
Previous studies of stained respiratory tract samples obtained by various methods indicate the
following relative diagnostic sensitivities: induced sputum <50% to >90% (the sensitivity depends on
the pathogen load and specimen quality, while the specificity depends on the experience of the
microbiologist or pathologist), bronchoscopy with BAL 90% to 99%, transbronchial biopsy 95% to 100%,
and open lung biopsy 95% to 100%.7
Patients with AIDS and pneumocystis pneumonia have a significantly increased number of
pneumocystis organisms in their lungs, with fewer neutrophils, than do patients with pneumocystis
pneumonia in the absence of AIDS. This greater organism burden results in a higher diagnostic yield of
induced sputum and bronchoalveolar lavage fluid to confirm pneumocystis pneumonia in patients with
AIDS as compared with other conditions associated with immunosuppression.8
Polymerase chain reaction (PCR) is an emerging method for diagnosing PCP. The sensitivity of
PCR for bronchoalveolar lavage appears to be high; the ability of PCR to distinguish colonization from
15
disease is less clear. 1,3s-D-glucan (a component of fungal cell walls) may be elevated in patients with
PCP, but the assay’s sensitivity and specificity for establishing a PCP diagnosis are problematic, and
other fungal diseases can produce elevation.7
Because certain processes produce similar clinical manifestations, a specific diagnosis of PCP
should be sought rather than relying on a presumptive diagnosis, especially in patients with moderate-
to-severe disease.7
Treatment can be initiated before making a definitive diagnosis because organisms persist in
clinical specimens for days or weeks after effective therapy is initiated.11
Management
Trimethoprim- Sulfamethoxazole (TMP-SMX) is the treatment of choice for PCP.10 The dose
must be adjusted for abnormal renal function. 13 Adding leucovorin to prevent myelosuppression during
acute treatment is not recommended because efficacy is questionable and some evidence exists for a
higher failure rate. Oral outpatient therapy with TMP-SMX is highly effective in patients with mild to
moderate disease.14 Alternative therapeutic regimens for mild-to-moderate disease include: dapsone
and TMP which may have efficacy similar to TMP-SMX and fewer side effects, but is less convenient
because of the number of pills; primaquine plus clindamycin; and atovaquone suspension, which is less
effective than TMP-SMX for mild-to-moderate disease but has fewer side effects. Whenever possible,
patients should be tested for glucose-6-phosphate dehydrogenase deficiency before primaquine or
dapsone is administered. 7
Alternative therapeutic regimens for patients with moderate-to-severe disease include
clindamycinprimaquine or IV pentamidine. Some clinicians prefer clindamycin-primaquine because of
its higher degree of efficacy and lesser toxicity compared with pentamidine. Aerosolized pentamidine
should not be used to treat PCP because its efficacy is limited and it is associated with more frequent
relapse.
Mutations associated with resistance to sulfa drugs have been documented, but their effect on
clinical outcome is uncertain. Patients who have PCP despite TMP-SMX prophylaxis usually can be
treated effectively with standard doses of TMP-SMX. Patients with documented or suspected PCP and
moderate to severe disease, defined by room air pO2 <70 mm Hg or Alveolar-arterial O2 gradient ≥35
mm Hg, should receive adjunctive corticosteroids as early as possible and certainly within 72 hours
after starting specific PCP therapy. Methylprednisolone at 75% of the respective prednisone dose can
be used if parenteral administration is necessary. 7
16
The recommended duration of therapy for PCP is 21 days.15 The probability and rate of
response to therapy depend on the agent used, number of previous PCP episodes, severity of
pulmonary illness, degree of immunodeficiency, timing of initiation of therapy and comorbidities. 7
The overall prognosis remains poor for patients who have such severe hypoxemia that
admission to an intensive care unit (ICU) is necessary. However, in recent years, such patients have
had much better survival than in the past, perhaps because of better management of comorbidities
and better supportive care. Because long-term survival is possible for patients in whom ART is
effective, individuals with AIDS and severe PCP should be offered ICU admission or mechanical
ventilation if their functional status is such that it would be appropriate, just as with HIV-uninfected
patients. In patients not on ART, ART should be initiated, when possible, within 2 weeks of diagnosis
of PCP. 7
17
the common practice is to use parenteral pentamidine or oral primaquine combined with intravenous
clindamycin. Cohort studies concluded that the combination of clindamycin and primaquine might be
the most effective regimen for salvage therapy, although no prospective clinical trials have evaluated
the optimal approach to patients who experience a therapy failure with TMP-SMX. 7
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